Mitotic bookmarking provides epigenetic persistence or plasticity for biological control and cancer.

Abstract

Mitotic bookmarking, the retention of regulatory proteins and lncRNAs on chromatin during mitosis, epigenetically sustains competency for phenotype-specific gene expression in progeny cells. Gene expression is predominantly suppressed during mitosis. Bookmarking provides the guidance for the resumption of gene expression in progeny cells that is obligatory for physiological control of lineage commitment, specialized cell structure and phenotypic function. While regulatory continuity is supported by the persistence of genome-associated regulatory complexes, altered bookmarking mediates plasticity for responsiveness to physiological cues. Bookmarking fidelity ensures genome integrity and controls expression of tumor suppressors and proto-oncogenes. Cancer-compromised aberrations in bookmarking results in transcriptional dysregulation and the initiation of tumor-associated processes.